EOSINOPHILIC BRONCHOPNEUMOPATHY

Canine eosinophilic bronchopneumopathy (EBP) is a disease characterised by eosinophilic infiltration of lung and bronchial mucosa that has traditionally been refered to as pulmonary infiltrates with eosinophilia (PIE). PIE is described in humans where the term includes a range of different allergic respiratory diseases, with variable clinical presentation. As in human, the syndrome is considered to be manifestations of immunological hypersensitivity. Therefore, an underlying antigen source is actively pursued in affected humans and dogs. Suspected and known causes of pulmonary hypersensitivities in humans and animals include fungi, molds, drugs, bacteria, and parasites. Canine EBP has been shown to be associated with heartworms, pulmonary parasites, variable chemical agents and drugs. Bacteria and fungi could also possibly play a role as an inciting agent in some cases of canine eosinophilic bronchopulmonary disease. However, in many cases, no underlying cause is found.

The role of inhaled allergens in EBP is still unclear. The mechanisms of pulmonary hypersensitivity are poorly understood in both human and veterinary medicine. In allergic respiratory diseases in humans, an imbalance of the lymphocyte subsets in the BALF, due to higher number of CD4⁺T cells together with lower percentage of CD8⁺T cells has been suggested to contribute to eosinophil accumulation, bronchial hyperresponsiveness and other symptoms. In the BALF of dogs with EBP, a similar imbalance has been shown; after treatment with glucocorticosteroids, the BALF T cell percentages returned to normal. Therefore the influx of eosinophils into the airway of dogs with EBP is thought to be at least in part mediated by cytokines derived from CD4⁺T cells. Canine EBP is thought to involve type I hypersensitivity mechanisms regulated by Th2 lymphocytes, although further studies of canine cytokines and chemokines should confirm this hypothesis.

Other immunological variables studied in dogs with eosinophilic bronchopneumopathy (EBP) include the determination of immunoglobulin concentrations both in the peripheral blood and in the bronchoalveolar lavage fluid (BALF). The findings suggest that serum and mucosal immunodeficiency do not underlie EBP.

Eosinophilic bronchopneumopathy is mostly diagnosed in young dogs. Siberian huskies and malamutes are predominantly affected but many breeds can be affected. Usually, the general condition is good, unless the disease is associated with concomittant bacterial bronchopneumonia. Clinical signs include mainly cough, gagging and retching. Cough, gagging and retching are symptoms present in 100% of the cases. In acute cases, gagging and retching are sometimes the main complaint, extending the differential diagnosis to dyspeptic problems. Dyspnea is a very frequent sign. Less commonly encountered sign are nasal discharge (about 50% of the affected dogs).

Diagnostic elements for the diagnosis of EBP include anamnetic factors (breed, young age, previous response to corticosteroids), clinical signs, radiographic and bronchoscopic findings, blood eosinophilia, tissue eosinophilic infiltration as demonstrated by cytological and histopathological examinations, response to adequate treatment, and also rests on exclusion of other pathologies. The most common radiographic findings are a mixed moderate to severe bronchointerstitial pattern. Alveolar infiltration can be noticed and can be related either eosinophilic alveolar infiltration or to bacterial pneumonia.

Bronchoscopy can reveal typical macroscopic features which include the presence of abundant yellow-green mucous or mucopurulent material, severe thickening of the mucosa with irregular or polypoid surface and in some cases partial airway closure during expiration. Peripheral blood eosinophilia is frequently (in about 60% of the cases) but not always observed. BALF or brush cytology demonstrate a marked eosinophilic component; frequently, more than 50% of the inflammatory cells are eosinophils. In most cases, eosinophilic infiltration of the bronchial mucosa can also be observed in biopsies.

The response to steroid therapy is generally very good, although achievement of total lack of symptoms is not always obtained. Cough and dyspnea improve generally within days of initiating the steroid treatment. Nasal discharge is sometimes more refractory to treatment. Initial therapy includes prednisolone and antibiotics when needed (in case of concomitant secondary bacterial bronchopneumonia). Prednisolone is initiated at a dosage of 1 mg/kg q 12h the first week; the same dose is given on alternate days during the second week, and then 1 mg/kg q24h on alternated days during the third week, followed by gradual decrease until maintenance dosage.The maintenance" dose of prednisolone range between 0.125 mg/kg and 0.5 mg /kg on alternate day, or even less regular administration schedules. Relapse frequently occurs within weeks to months after drug discontinuation although some dogs may remain asymptomatic after discontinuation. A successful clinical response of the disease following glucocorticoid therapy corresponds to a resolution of the eosinophilic infiltration. So far, hyposensitivation therapy does not appear to be the treatment of choice and should not be advised without concomitant glucocorticoid therapy.

Achievement of total lack of symptoms is rare. The poorest responses to treatment occur in cases that are irregularly treated, with repeated abrupt cessation of high doses of medication without tapering, or with irregular parenteral administration of repository steroid injections. Therefore, a major goal of management is client education. Regular oral corticotherapy must be used on alternate days with progressive tapering of the dose, rather than irregular oral or parenteral high doses. There seems to be no relationship between the duration of clinical signs, the severity of eosinophilic infiltration and the response to treatment. If the treatment is adequate, the quality of life and life time are good, even though the animal has to be treated longlife.